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1
Nguyen, Thao P., Mansoureh Eghbali, and Sally Ann Frautschy, eds. Oxidative Stress in Myocardial and Neural Remodeling. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88966-657-7.
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2
Sherman, Jerald. Cardiac Remodeling: Molecular Mechanisms, Treatment and Clinical Implications. Nova Science Publishers, Incorporated, 2016.
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3
K, Singal Pawan, ed. Cardiac remodeling and failure. Boston: Kluwer Academic Pub., 2003.
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4
Dhalla, Naranjan S., Pawan K. Singal, Ian M. C. Dixon, and Lorrie A. Kirshenbaum. Cardiac Remodeling and Failure. Springer, 2012.
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6
1945-, Hori M., Janicki Joseph S, and Maruyama Yukio 1941-, eds. Cardiac-vascular remodeling and functional interaction. Tokyo: Springer, 1997.
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7
1941-, Maruyama Yukio, Hori M. 1945-, and Janicki Joseph S, eds. Cardiac-vascular remodeling and functional interaction. Tokyo: Springer, 1997.
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8
Dilsizian, Vasken, Ines Valenta, and Thomas H. Schindler. Myocardial Viability Assessment. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199392094.003.0021.
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Heart failure may be a consequence of ischemic or non-ischemic cardiomyopathy. Etiologies for LV systolic dysfunction in ischemic cardiomyopathy include; 1) transmural scar, 2) nontransmural scar, 3) repetitive myocardial stunning, 4) hibernating myocardium, and 5) remodeled myocardium. The LV remodeling process, which is activated by the renin-angiotensin system (RAS), stimulates toxic catecholamine actions and matrix metalloproteinases, resulting in maladaptive cellular and molecular alterations5, with a final pathway to interstitial fibrosis. These responses to LV dysfunction and interstitial fibrosis lead to progressive worsening of LV function. Established treatment options for ischemic cardiomyopathy include medical therapy, revascularization, and cardiac transplantation. While there has been continuous progress in the medical treatment of heart failure with beta-blockers, angiotensin-converting enzyme (ACE) inhibition, angiotensin II type 1 receptor (AT1R) blockers, and aldosterone to beneficially influence morbidity and mortality, the 5-years mortality rate for heart failure patients remains as high as 50%. Revascularization procedures include percutaneous transluminal coronary artery interventions (PCI) including angioplasty and endovascular stent placement and coronary artery bypass grafting (CABG). Whereas patents with heart failure due to non-coronary etiologies may best benefit from medical therapy or heart transplantation, coronary revascularization has the potential to improve ventricular function, symptoms, and long term survival, in patients with heart failure symptoms due to CAD and ischemic cardiomyopathy.
9
(Editor), Pawan K. Singal, Ian M.C. Dixon (Editor), Lorrie A. Kirshenbaum (Editor), and Naranjan S. Dhalla (Editor), eds. Cardiac Remodeling and Failure (Progress in Experimental Cardiology). Springer, 2003.
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10
Hausenloy, Derek, and Derek Yellon, eds. Coronary No-Reflow and Microvascular Obstruction. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0005.
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• Following an AMI, the restoration of TIMI III coronary blood flow using thrombolytic therapy or primary percutaneous coronary intervention does not guarantee actual myocardial perfusion• In 40–60% of reperfused AMI cases, myocardial perfusion is impeded at the level of the capillaries due to microvascular obstruction (MVO)- a phenomenon termed coronary no-reflow• The presence of coronary no-reflow can be detected as impaired myocardial perfusion using non-invasive imaging modalities such as nuclear myocardial perfusion scanning, myocardial contrast echocardiography or contrast-enhanced cardiac magnetic resonance imaging• The presence of microvascular obstruction post-AMI is associated with a larger infarct size, impaired LV ejection fraction, adverse LV remodelling and poorer clinical outcomes• Current treatment strategies include; vasodilator therapy such as adenosine, calcium-channel blockers, and nitrates; distal protection to prevent microemboli; and glycoprotein IIb/IIIa inhibitors• Novel treatment strategies are required to prevent and treat coronary no-reflow, thereby improving myocardial perfusion, reducing myocardial infarct size, preserving LV ejection fraction, preventing LV remodeling and improving clinical outcomes.
11
Greenberg, Barry. Cardiac Remodeling: Mechanisms and Treatment (Fundamental and Clinical Cardiology). Informa Healthcare, 2005.
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12
Antoine, Lafont, and Topol Eric J. 1954-, eds. Arterial remodeling: A critical factor in restenosis. Boston: Kluwer Academic Publishers, 1997.
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13
Adam, Jonathan Eliot. The effect of matrix metalloproteinase inhibition on post-myocardial infarction cardiac function, remodeling and gene expression. 2005.
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14
Adam, Jonathan Eliot. The effect of matrix metalloproteinase inhibition on post-myocardial infarction cardiac function, remodeling and gene expression. 2005.
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15
Vimalesvaran, Kavitha, and Michael Marber. Myocardial Remodelling after Myocardial Infarction. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0031.
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This chapter focuses on myocardial remodelling, a process that affects the heart’s shape, structure, and function, following myocardial injury (MI). Post-MI remodelling can be divided into three phases, with the first phase 0–72 hours beginning at the time of ischaemic injury, the second phase 72 hours to 6 weeks, and the third and last phase 6 weeks and beyond. During post-infarction remodelling, hypertrophy is an adaptive response that compensates for the increased load, reduces the effect of progressive dilatation, and balances contractile function. The chapter discusses the factors involved in ventricular remodelling and its association with heart failure progression. The effects of therapies designed to prevent or attenuate post-infarction left ventricular remodelling, with reference to the pathophysiological mechanisms involved, are then considered. Therapies specifically discussed include angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), β-adrenoreceptor blockers, and aldosterone receptor antagonists.
16
Arterial Remodeling: A Critical Factor in Restenosis (Developments in Cardiovascular Medicine). Springer, 1997.
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17
Joy, Brenda Margaret. The effect of early and late post-myocardial administration of Batimastat, a matrix metalloproteinase inhibitor, on left ventricular function and remodeling. 2002.
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18
Opie, Lionel. Optimal Medical Therapy Post-AMI. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0006.
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• The management of an acute myocardial infarction can be divided into four phases: (a) The initial acute ischaemia causes severe prolonged chest pain when the patient is rushed to a Coronary or Intensive Care Unit; (b) Within the next few hours as ischaemia changes into infarction, the aim at this step is to restore blood flow in the occluded artery by thrombolysis or by percutaneous coronary intervention (PCI); (c) Next, the infarct is established and the left ventricle undergoes early remodeling; (d) Finally, follows the post-AMI post-hospital phase when continued left ventricular remodeling takes place• The therapeutic management of each of these steps can be optimized using appropriate medical therapy including antiplatelet and antithrombotic therapy, beta-blockers, ACE-inhibitors and angiotensin receptor blockers, lipid-lowering drugs, aldosterone antagonists, omega-3 fatty acids and so on.
19
Sutton, John. Left Ventricular Remodelling After Acute Myocardial Infarction. Science Press, 1996.
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20
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0045.
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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
21
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_001.
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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
22
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_002.
Full textAbstract:
Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
23
López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_003.
Full textAbstract:
Mechanical complications after an acute infarction involve different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies occurring in <1% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment (Ibanez et al, 2017). Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
24
D’Andrea, Antonello, André La Gerche, and Christine Selton-Suty. Systemic disease and other conditions: athlete’s heart. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0055.
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The term ‘athlete’s heart’ refers to the structural, functional, and electrical adaptations that occur as a result of habitual exercise training. It is characterized by an increase of the internal chamber dimensions and wall thickness of both atria and ventricles. The athlete’s right ventricle also undergoes structural, functional, and electrical remodelling as a result of intense exercise training. Some research suggests that the haemodynamic stress of intense exercise is greater for the right heart and, as a result, right heart remodelling is slightly more profound when compared with the left heart. Echocardiography is the primary tool for the assessment of morphological and functional features of athlete’s heart and facilitates differentiation between physiological and pathological LV hypertrophy. Doppler myocardial and strain imaging can give additional information to the standard indices of global systolic and diastolic function and in selected cases cardiac magnetic resonance imaging may help in the diagnosis of specific myocardial diseases among athletes such as hypertrophic cardiomyopathy, dilated cardiomyopathy, or arrhythmogenic right ventricular cardiomyopathy.
25
Menasché, Philippe. Stem Cell Therapy Post-AMI. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199544769.003.0010.
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• Experimental studies suggest that bone marrow-derived stem cells can improve function of infarcted myocardium• This benefit seems to involve paracrine signalling and limitation of left ventricular remodelling rather than true regeneration of cardiomyocytes from donor cells• These experimental findings have been translated in the clinical setting into significant, although moderate, improvements in cardiac function and LV remodelling but the extent to which these benefits impact on event-free long term survival remains to be determined• Optimisation of this therapeutic strategy will require a more comprehensive characterisation of cell functionality and an improvement in the methods used in cell transfer, engraftment, survival and integration.
26
Pierard, Luc A., and Lauro Cortigiani. Stress echocardiography: diagnostic and prognostic values and specific clinical subsets. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0015.
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Stress echocardiography is a widely used method for assessing coronary artery disease, due to its high diagnostic and prognostic value. While inducible ischaemia predicts an unfavourable outcome, its absence is associated with a low risk of future cardiac events. The method provides superior diagnostic and prognostic information than standard exercise electrocardiography and perfusion myocardial imaging in specific clinical subsets, such as women, hypertensive patients, and patients with left bundle branch block. Stress echocardiography allows effective risk assessment also in the diabetic population. The evaluation of coronary flow reserve of the left anterior descending artery by transthoracic Doppler adds diagnostic and prognostic information to that of standard stress test. Stress echocardiography is indicated in the cases when exercise electrocardiography is unfeasible, uninterpretable or gives ambiguous result, and when ischaemia during the test is frequently a false-positive response, as in hypertensive patients, women, and patients with left ventricular hypertrophy. Viability detection represents another application of stress echocardiography. The documentation of a large amount of viable myocardium predicts improved ejection fraction, reverse remodelling, and improved outcome following revascularization in patients with ischaemic cardiomyopathy. Moreover, stress echocardiography can aid significantly in clinical decision-making in patients with valvular heart disease through dynamic assessment of primary or secondary mitral regurgitation, transvalvular gradients, and pulmonary artery systolic pressure, as well as before vascular surgery due to the excellent negative predictive value. Finally, stress echocardiography allows effective risk stratification in patients with hypertrophic cardiomyopathy through evaluation of inducible ischaemia, coronary flow reserve, and intraventricular gradient.
27
Ruiz-Villalba, Adrián, Nikolaos Frangogiannis, and José Maria Pérez-Pomares. Origin and diversity of cardiac fibroblasts: developmental substrates of adult cardiac fibrosis. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0012.
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Cardiac connective tissues are primarily formed by cardiac fibroblasts (CF) of diverse embryonic origins. Whereas CF specific roles in cardiac morphogenesis remain under-researched, their involvement in adult cardiac fibrosis is clinically relevant. Cardiac fibrosis is a common element of several chronic cardiac conditions characterized by the loss of ventricular wall mechanical function, ultimately driving to heart failure. In the ischaemic heart early reparative fibrosis evidences the very restricted regenerative potential of the myocardium. In non-ischaemic diseases fibrosis is activated by unknown signals. We summarize current knowledge on the origin of CFs and their developmental roles, and discuss the differential disease-dependent response of different CF subpopulations to various pathological stimuli. We also describe the characteristic cell-cell and cell-matrix interactions that determine the fibrotic remodelling of the myocardium. We analyse experimental models for the study of cardiac fibrosis, and suggest future directions in the search for new markers and therapeutic targets.
28
Walsh, David. Attenuation of ventricular remodelling post myocardial infarction: A systematic review of the evidence of treatment with angiotensin converting enzyme inhibitors, nitrates and beta blockers. 1999.
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29
Paneni, Francesco, and Massimo Volpe. Co-morbidity (HFrEF and HFpEF): hypertension. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198784906.003.0415_update_001.
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Hypertensive heart disease is a major cause of heart failure (HF) and mortality. Hypertension precedes HF occurrence in 75% of cases, and carries a sixfold increase in HF risk as compared to non-hypertensive individuals. Most importantly, a minority of patients survive 5 years after the onset of hypertensive HF. In hypertensive patients, the heart may present different patterns of adaptive remodelling: concentric remodelling, concentric hypertrophy, and eccentric hypertrophy. Although most hypertensive patients are at high risk of developing concentric hypertrophy, a growing proportion of subjects display a concentric-to-eccentric progression eventually leading to left ventricular dilation and systolic dysfunction. Several factors including myocardial ischaemia, ethnicity, genetic background, history of diabetes, and blood pressure pattern may significantly influence the pathway from hypertension to left ventricular dilation. Patients with a concentric hypertrophy usually develop HF with preserved ejection fraction (HFpEF), whereas those with an eccentric (dilated) phenotype develop HF with reduced ejection fraction (HFrEF). Lowering blood pressure has a striking effect in reducing the risk of HF. Although available antihypertensive drugs are all successful in lowering blood pressure, angiotensin-converting enzyme inhibitors, angiotensin receptor blocker (ARBs), and diuretics are more effective than other drug classes in preventing HF. The combination of the neprilysin inhibitor sacubitril with the ARB valsartan (LCZ696) has recently been shown to be highly effective in reducing HF-related outcomes in hypertensive subjects. An individualized treatment scheme taking into account blood pressure levels, type of HF (HFpEF or HFrEF), and relevant co-morbidities (i.e. renal disease, diabetes) is currently the best approach to improve morbidity and mortality in hypertensive patients with HF.
30
London, Gerard M. Cardiovascular complications in end-stage renal disease patients. Edited by Jonathan Himmelfarb. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0268.
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Cardiovascular complications are the predominant cause of death in patients with end-stage renal disease (ESRD). The high incidence of cardiovascular complications results from pathology present before ESRD (generalized atherosclerosis, diabetes, hypertension) and an additive effect of multiple factors including haemodynamic overload and metabolic and endocrine abnormalities more or less specific to uraemia or its treatment modalities. These disorders are usually associated and can exacerbate each other. While ischaemic heart disease is a frequent cause of cardiac death, heart failure and sudden death are the most frequent causes of death in ESRD. Cardiomyopathy of overload with development of left ventricular hypertrophy and fibrosis are the most characteristic alterations and major determinants of prognosis. Left ventricular hypertrophy may result in systolic and/or diastolic dysfunction and is a risk factor for arrhythmias, sudden death, heart failure, and myocardial ischaemia. Arterial disease, whether due to atherosclerosis or arteriosclerosis (or both), represents a major contributory factor to the cardiovascular complications. Arterial disease may result in ischaemic complications (ischaemic heart disease, peripheral artery diseases) or arterial stiffening with direct consequences on left ventricular afterload, decreased coronary perfusion, and microvascular abnormalities (inward remodelling and microvessel rarefaction).
31
Yilmaz, Ali, and Anca Florian. Myocarditis: imaging techniques. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0367.
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The clinical presentation of myocarditis is multifaceted and electrocardiogram (ECG) changes as well as biomarkers tend to be non-specific. Therefore, the diagnosis of myocarditis can be challenging and should be based on an integrated approach including patient history, physical examination, non-invasive tests such as ECG and serum biomarkers, and non-invasive cardiac imaging. As myocarditis may lead to global ventricular dysfunction, regional wall motion abnormalities, and/or diastolic dysfunction, echocardiography should be routinely performed. However, hallmarks of acute myocarditis comprise structural changes such as cardiomyocyte swelling, an increase in extracellular space and water content, accumulation of inflammatory cells, potential necrosis or apoptosis of cardiomyocytes, and myocardial remodelling with fibrotic tissue replacement that can be depicted by cardiovascular magnetic resonance. Nuclear techniques are still not routinely recommended for the work-up of myocarditis—with the possible exception of suspected sarcoidosis—due to limited data, limited diagnostic specificity, limited availability, and risk from radiation exposure. This chapter focuses on those non-invasive cardiac imaging techniques that are used in daily clinical practice for work-up of suspected myocarditis. However, as research continues and novel imaging techniques become available, it is hoped that even more accurate and timely diagnosis of myocarditis will be possible in the near future.
32
Arbustini, Eloisa, Valentina Favalli, Alessandro Di Toro, Alessandra Serio, and Jagat Narula. Classification of cardiomyopathies. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0348.
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For over 50 years, the definition and classification of cardiomyopathies have remained anchored in the concept of ventricular dysfunction and myocardial structural remodelling due to unknown cause. The concept of idiopathic was first challenged in 2006, when the American Heart Association classification subordinated the phenotype to the aetiology. Cardiomyopathies were classified as genetic, acquired, and mixed. In 2008, the European Society of Cardiology proposed a phenotype-driven classification that separated familial (genetic) from non-familial (non-genetic) forms of cardiomyopathy. Both classifications led the way to a precise phenotypic and aetiological description of the disease and moved away from the previously held notion of idiopathic disease. In 2013, the World Heart Federation introduced a descriptive and flexible nosology—the MOGE(S) classification—describing the morphofunctional (M) phenotype of cardiomyopathy, the involvement of additional organs (O), the familial/genetic (G) origin, and the precise description of the (a)etiology including genetic mutation, if applicable (E); reporting of functional status such as American College of Cardiology/American Heart Association stage and New York Heart Association classification (S) was left optional. MOGE(S) is a bridge between the past and the future. It allows description of comprehensive phenotypic data, all genetic and non-genetic causes of cardiomyopathy, and incorporates description of familial clustering in a genetic disease. MOGE(S) is the instrument of precision diagnosis for cardiomyopathies. The addition of the early and unaffected phenotypes to the (M) descriptor outlines the clinical profile of an early affected family member; the examples include non-dilated hypokinetic cardiomyopathy in dilated cardiomyopathy and septal thickness (13–14 mm) in hypertrophic cardiomyopathy classes.